Abstract

The present investigation was undertaken to examine the influence of super oxide anion generator hydroquinone and the superoxide anion scavenger superoxide dismutase (SOD) on the neurally mediated relaxation of the internal and sphincter (IAS). The studies were performed in vitro on IAS smooth muscle strips of opossums. Neural stimulation with appropriate parameters of electrical field stimulation is known to cause IAS relaxation by the activation of nonadrenergic noncholinergic inhibitory neurons. Hydroquinone caused a concentration-dependent suppression of IAS relaxation in response to neural stimulation. The suppression of the IAS relaxation was reversed by SOD in a concentration-dependent manner. The fall in the IAS tension by nitric oxide (NO) was also suppressed by hydroquinone and reversed by SOD. SOD alone caused an augmentation of the fall in the IAS tension by NO. The fall in the IAS tension in response to the candidate inhibitory neurotransmitter vasoactive intestinal polypeptide was not modified by SOD in the basal state. Hydroquinone, however, caused a significant suppression of vasoactive intestinal polypeptide-induced fall in the IAS tension which was reversed by SOD. The fall in the resting IAS tension by the directly acting smooth muscle relaxants, beta adrenoceptor agonist isoproterenol and atrial natriuretic factor were not significantly modified by hydroquinone or SOD. From the present data we conclude: NO or an NO-like factor plays a significant role in the nonadrenergic noncholinergic nerve-mediated IAS relaxation.

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